245 Genetic parameters for reproductive performance traits before, during, and after Porcine Reproductive and Respiratory Syndrome outbreaks in a purebred maternal line.

Abstract Porcine reproductive and respiratory syndrome (PRRS) is a viral disease with a significant impact on the swine industry worldwide. Therefore, breeding for improved PRRS resistance and resilience is of great interest in swine breeding programs. This study aimed to first detect the PRRS outbreak periods in four farms based on sow reproductive performance records and assess the impact of PRRS outbreaks on the genetic variability of reproductive traits before, during, and after the outbreaks. We analyzed data from 42,308 farrowing events of 13,576 Large White sows across three farms in the USA and one in Spain with reported PRRS outbreaks. The traits evaluated included total number of piglets born (TNB), number of piglets born alive (NBA), number of piglets born dead (NBD), and number of piglets weaned (NW). Pedigree records were available for each sow, and 25K single nucleotide polymorphism genotype data was available for each sire (n = 483). The phenotypic dataset was divided into three periods: before, during, and after the PRRS outbreak, based on weekly averages of NBA, NBD, and NW. Variance components and heritability estimates were obtained from single-trait analyses for each period separately. Genetic correlations for each trait across periods were estimated using bivariate analyses. The model used for the analyses was a repeatability model, and all analyses were performed using the single-step genomic Best Linear Unbiased Prediction approach with the BLUPF90+ software. During the PRRS outbreak period, there was a significant increase in NBD, while NBA and NW decreased. Heritability estimates before, during, and after the PRRS break were: 0.10 ± 0.01, 0.13 ± 0.03, and 0.14 ± 0.02 (TNB); 0.09 ± 0.01, 0.09 ± 0.02, and 0.07 ± 0.02 (NBA); 0.07 ± 0.01, 0.07 ± 0.02, and 0.17 ± 0.02 (NBD); and 0.06 ± 0.01, 0.06 ± 0.01, and 0.16 ± 0.03 (NW), respectively. Genetic correlations across periods ranged from 0.94 to 0.99 (TNB); 0.72 to 0.95 (NBA); 0.73 to 0.89 (NBD); and from 0.47 to 0.69 (NW). In conclusion, PRRS outbreaks can be detected by analyzing phenotypic variation in longitudinal reproductive performance data. Results show that reproductive performance is heritable, whether evaluated before, during, or after a PRRS break. However, the range in genetic correlations across phases indicates that a given trait may not be controlled by the same set of genes before vs. during vs. after PRRS exposure. These findings suggest that genetic selection for enhanced reproductive performance in the absence of PRRS is expected to enhance resilience to PRRS following an outbreak; however, collecting data under challenge should capture additional genetic variation in PRRS resilience.